Prestin is the molecular motor which changes th`e length of the outer hair cells of the vertebrate cochlea to increase the sensitivity and specificity of hearing. Loss of prestin decreases the sensitivity of hearing in mice. The following approaches will be used to determine the role of a possible Drosophila homologue of prestin (dpres): 1) In situ hybridization will be used to determine the expression pattern of dpres in Drosophila embryos. To provide confirmation of in situ hybridization data and allow visualization of the dpres expression pattern in adults, the GAL4 transcriptional activator will be regulated by the upstream regulatory region of dpres allowing lacZ or GFP reporter genes to be expressed in the dpres pattern. 2) Since there are no mutations, P-element insertions, or expressed sequence tags reported in the dpres gene, targeted homologueous recombination will be used to create a loss of function allele of dpres. Mutants will be assayed for defects in sensory systems using behavioral and electrophysiological tests. 3) Expression of dpres using the UAS-Gal4 system will be used to determine where dpres must be expressed to rescue dpres loss of function phenotypes. Dpres will also be expressed ectopically to look for gain of function phenotypes identified by behavioral and/or electrophysiological assays. The expression pattern of dpres, combined with the phenotypes of loss and gain of function, will illuminate the role of dpres in Drosophila sensory systems and provide a base from which to examine the structure and function of prestin to better understand its role in Drosophila and vertebrate hearing.